m^(6)A去甲基化酶ALKBH5与肿瘤发生、发展的研究进展  

Research Progress of m^(6)A Demethylase ALKBH5 and Tumorigenesis and Development

作　　者：邓云洋 孙达欣 梁万旺 黄丰泽 DENG Yunyang;SUN Daxin;LIANG Wanwang;HUANG Fengze(Department of Breast and Thyroid Surgery,Affiliated Hospital of Guilin Medical University,Guilin 541000,China)

机构地区：[1]桂林医学院附属医院乳甲外科,广西桂林541000

出　　处：《医学综述》2022年第13期2608-2613,共6页Medical Recapitulate

摘　　要：N^(6)-甲基腺嘌呤(m^(6)A)修饰是指在腺苷酸6位的N原子上插入一个甲基取代基。m^(6)A修饰在甲基转移酶、去甲基化酶和解读器蛋白共同调控下完成,其修饰调控紊乱可影响基因的表达,进而通过调节肿瘤生物学过程(如增殖、迁移、侵袭、转移)在多种肿瘤中发挥重要作用。ALKB同系物5作为m^(6)A修饰中的一种重要去甲基化酶,在不同肿瘤中的表达水平、目标基因以及发挥的作用均不同,且其作用机制尚未明确,未来仍需进一步阐明其具体机制,进而为肿瘤的分子靶向治疗提供新线索。N^(6)-methyladenine(m^(6)A)modification refers to the insertion of a methyl substituent into the 6-position N atom of adenosine.m^(6)A modification is completed under the joint regulation of methyltransferase,demethylase and reader protein,and its modification and regulation disorder can affect gene expression,thus playing an important role in a variety of tumors by regulating various tumor biological processes(such as proliferation,migration,invasion and metastasis).ALKB homologous 5,as an important demethylation enzyme in m^(6)A modification,has different expression levels,target genes and roles in different tumors,and its mechanism of action is not clear yet.Further elucidation of its specific mechanism is still needed in the future,thus providing new clues for molecular targeted therapy of tumors.

关 键 词：肿瘤 N^(6)-甲基腺嘌呤修饰 ALKB同系物5 

分 类 号：R73[医药卫生—肿瘤]